Lung adenocarcinoma (LUAD) is the most important histological type of lung cancer. We aimed to identify the role of long noncoding RNA family with sequence similarity 201-member A (FAM201A) in the occurrence and development of LUAD. The expressions of FAM201A in LUAD tissues and cells were determined via reverse transcription-quantitative polymerase chain reaction. The effects of FAM201A knockdown on LUAD cell malignant phenotypes were examined by cell counting kit-8, 5-ethynyl-2'-deoxyuridine, flow cytometry, transwell assay and wound healing assay. The underlying mechanism by which FAM201A regulated LUAD progression was also studied. Nude mice LUAD xenograft model was constructed, to explore the in vivo effect of FAM201A. Our results showed that the FAM201A expression in LUAD tissues and cell lines was notably higher than normal tissues and cells. Downregulation of FAM201A suppressed the cell proliferation, migration and invasion and promoted the cell apoptosis in LUAD cells. While, FAM201A overexpression showed tumorigenesis effect on LUAD cells. Moreover, we demonstrated that FAM201A affected LUAD progression via targeting miR-7515 to promote GLO1 expression. FAM201A downregulation also suppressed LUAD development in vivo experiment. Our results indicated that FAM201A was an oncogene in LUAD and might be a novel therapeutic target for LUAD.
Keywords: FAM201A; Lung adenocarcinoma; invasion; migration; proliferation.
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